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Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C
Author(s) -
Hézode Christophe,
RoudotThoraval Françoise,
Nguyen Son,
Grenard Pascale,
Julien Boris,
Zafrani ElieSerge,
Pawlostky JeanMichel,
Dhumeaux Daniel,
Lotersztajn Sophie,
Mallat Ariane
Publication year - 2005
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.20733
Subject(s) - cannabis , fibrosis , medicine , steatosis , cannabinoid receptor , gastroenterology , liver biopsy , hepatitis c virus , hepatitis c , hepatic fibrosis , cannabinoid , immunology , biopsy , receptor , virus , psychiatry , agonist
Cannabinoids present in Cannabis sativa (marijuana) exert biological effects via cannabinoid receptors CB1 and CB2. We recently demonstrated that CB1 and CB2 receptors regulate progression of experimental liver fibrosis. We therefore investigated the impact of cannabis smoking on fibrosis progression rate in patients with chronic hepatitis C (CHC). Two hundred seventy consecutive untreated patients with CHC of known duration undergoing liver biopsy were studied. Demographic, epidemiological, metabolic, and virological data were recorded, and detailed histories of cannabis, alcohol, and tobacco use over the span of hepatitis C virus infection were obtained. Fibrosis stage, steatosis, and activity grades were scored according to Metavir system. Patients were categorized as noncannabis users (52.2%), occasional users (14.8%), or daily users (33.0%), and the relationship between cannabis use and fibrosis progression rate (FPR) or fibrosis stage was assessed. On multivariate analysis, six factors were independently related to a FPR greater than 0.074 (median value of the cohort): daily cannabis use (OR = 3.4 [1.5‐7.4]), Metavir activity grade A2 or higher (OR = 5.4 [2.9‐10.3]), age at contamination of more than 40 years (OR = 10.5 [3.0‐37.1]), genotype 3 (OR = 3.4 [1.5‐7.7]), excessive alcohol intake (OR = 2.2 [1.1‐4.5]), and steatosis (OR = 2.0 [1.0‐4.1]). Daily cannabis use was also an independent predictor of a rapid FPR (>0.15) (OR = 3.6 [1.5‐7.5]). Finally, severe fibrosis (≥F3) was also predicted by daily cannabis use (OR = 2.5 [1.1‐5.6]; P = .034), independently of Metavir activity grade, excessive alcohol intake, age at liver biopsy, steatosis, and tobacco smoking. In conclusion , daily cannabis smoking is significantly associated with fibrosis progression during CHC. Patients with ongoing CHC should be advised to refrain from regular cannabis use. (H EPATOLOGY 2005;.)